ArticlePloS one2016
Effects of Cigarette Smoke Condensate on Oxidative Stress, Apoptotic Cell Death, and HIV Replication in Human Monocytic Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
42 citing papers in PubMed, 65 citations in OpenAlex.
- Article
- HIV-HPV interactions via extracellular vesicles among tobacco smokers and nonsmokers.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- LM11A-31, a modulator of p75 neurotrophin receptor, suppresses HIV-1 replication and inflammatory response in macrophages.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- The impacts of tobacco and nicotine on HIV-1 infection, inflammation, and the blood-brain barrier in the central nervous system.Frontiers in pharmacology · 2024Review
- Resveratrol and its analogs suppress HIV replication, oxidative stress, and inflammation in macrophages.NeuroImmune pharmacology and therapeutics · 2023Article
- Smooth Muscle Cell Phenotypic Switch Induced by Traditional Cigarette Smoke Condensate: A Holistic Overview.International journal of molecular sciences · 2023Article
- E-Cigarette Aerosol Condensate Leads to Impaired Coronary Endothelial Cell Health and Restricted Angiogenesis.International journal of molecular sciences · 2023Article
- Extracellular vesicles released from macrophages modulates interleukin-1β in astrocytic and neuronal cells.Scientific reports · 2023Article
- Article
- Targeting the alternative oxidase (AOX) for human health and food security, a pharmaceutical and agrochemical target or a rescue mechanism?The Biochemical journal · 2022Review
- Cigarette smoke-induced extracellular vesicles from dendritic cells alter T-cell activation and HIV replication.Toxicology letters · 2022Article
- Effect of benzo(a)pyrene on oxidative stress and inflammatory mediators in astrocytes and HIV-infected macrophages.PloS one · 2022Article
- HIV-1 Drug Resistance Profiles of Low-Level Viremia Patients and Factors Associated With the Treatment Effect of ART-Treated Patients: A Cross-Sectional Study in Jiangsu, China.Frontiers in public health · 2022Article
- Drugs of Abuse and Their Impact on Viral Pathogenesis.Viruses · 2021Review
- Smoking and Human Immunodeficiency Virus 1 Infection Promote Retention of CD8American journal of respiratory cell and molecular biology · 2021Article
- Nicotine self-administration with menthol and audiovisual cue facilitates differential packaging of CYP2A6 and cytokines/chemokines in rat plasma extracellular vesicles.Scientific reports · 2021Article
- Curcumin Suppresses the Lipid Accumulation and Oxidative Stress Induced by Benzo[a]pyrene Toxicity in HepG2 Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Anti-HIV Activity of Cucurbitacin-D against Cigarette Smoke Condensate-Induced HIV Replication in the U1 Macrophages.Viruses · 2021Article
- The Restorative Effect of Red Guava (Veterinary medicine international · 2021Article
- Overview on Interactive Role of Inflammation, Reactive Oxygen Species, and Calcium Signaling in Asthma, COPD, and Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
While cigarette smoking is prevalent amongst HIV-infected patients, the effects of cigarette smoke constituents in cells of myeloid lineage are poorly known. Recently, we have shown that nicotine induces oxidative stress through cytochrome P450 (CYP) 2A6-mediated pathway in U937 monocytic cells. The present study was designed to examine the effect of cigarette smoke condensate (CSC), which contains majority of tobacco constituents, on oxidative stress, cytotoxicity, expression of CYP1A1, and/or HIV-1 replication in HIV-infected (U1) and uninfected U937 cells. The effects of CSC on induction of CYP1 enzymes in HIV-infected primary macrophages were also analyzed. The results showed that the CSC-mediated increase in production of reactive oxygen species (ROS) in U937 cells is dose- and time-dependent. Moreover, CSC treatment was found to induce cytotoxicity in U937 cells through the apoptotic pathway via activation of caspase-3. Importantly, pretreatment with vitamin C blocked the CSC-mediated production of ROS and induction of caspase-3 activity. In U1 cells, acute treatment of CSC increased ROS production at 6H (>2-fold) and both ROS (>2 fold) and HIV-1 replication (>3-fold) after chronic treatment. The CSC mediated effects were associated with robust induction in the expression of CYP1A1 mRNA upon acute CSC treatment of U937 and U1 cells (>20-fold), and upon chronic CSC treatment to U1 cells (>30-fold). In addition, the CYP1A1 induction in U937 cells was mediated through the aromatic hydrocarbon receptor pathway. Lastly, CSC, which is known to increase viral replication in primary macrophages, was also found to induce CYP1 enzymes in HIV-infected primary macrophages. While mRNA levels of both CYP1A1 and CYP1B1 were elevated following CSC treatment, only CYP1B1 protein levels were increased in HIV-infected primary macrophages. In conclusion, these results suggest a possible association between oxidative stress, CYP1 expression, and viral replication in CSC-treated cells of myeloid lineage. This study warrants a closer examination of the role of CYP1B1 in smoking-mediated enhanced HIV replication.
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